title: Effects of hypertonic saline and dextran 70 on cardiac contractility after hemorrhagic shock.
abstract: OBJECTIVE
  The effects of a bolus of 7.5% NaCl-6% dextran 70 (HSD) on cardiac contractility were evaluated in anesthetized sheep with hemorrhagic shock.
  
  
  BACKGROUND
  HSD has been shown to be effective at resuscitation in cases of hypovolemia caused by hemorrhage. Common hemodynamic findings after the injection of HSD in hemorrhagic shock are the restoration of cardiac output, increased blood pressure, and improvement of peripheral circulation. Some mechanisms by which HSD maintains circulation in hemorrhagic shock have been proposed: rapid shift of fluid from intracellular to extracellular space, improved peripheral perfusion, and increased cardiac contractility. Conflicting data exist, however, regarding the positive effect of HSD on cardiac contractility after hemorrhagic shock.
  
  
  METHODS
  Hemorrhagic shock was induced by shedding mean blood volume of 31.4 mL/kg, and mean blood pressure was maintained at 50 mm Hg for 30 minutes. The HSD group (n = 6) received HSD (4 mL/kg), and the saline group (n = 6) received normal saline (40 mL/kg) after shock. Cardiac functions were measured in both groups using the left ventricular end-systolic pressure-volume relationship and preload recruitable stroke work during the experimental period: before shock, immediately after the resuscitation, and 2 hours after resuscitation.
  
  
  RESULTS
  Hemodynamic parameters in both groups demonstrated similar changes throughout the experimental period without significant difference between the two groups. Not only the slopes of end-systolic pressure-volume relationship and preload recruitable stroke work but also their placements did not result in any significant differences between the groups.
  
  
  CONCLUSIONS
  HSD seems to be an effective resuscitation fluid after hemorrhagic shock because the volume required to maintain circulation is smaller than that of normal saline. Our data, however, show that HSD does not enhance cardiac contractility after hemorrhagic shock.
authors.affiliation: Department of Emergency and Critical Care Medicine, St. Luke's International Hospital, Tokyo, Japan. qqryukoh@xa2.so-net.or.jp
authors.forename: R
authors.initials: R
authors.lastname: Ogino
authors.forename: K
authors.initials: K
authors.lastname: Suzuki
authors.forename: M
authors.initials: M
authors.lastname: Kohno
authors.forename: M
authors.initials: M
authors.lastname: Nishina
authors.forename: A
authors.initials: A
authors.lastname: Kohama
mesh_terms: D000818:Animals; D003911:Dextrans / Q000627:therapeutic use*; D004195:Disease Models, Animal; D004338:Drug Combinations; D004353:Drug Evaluation, Preclinical; D005440:Fluid Therapy / Q000379:methods*; D006801:Humans; D009200:Myocardial Contraction / Q000187:drug effects*; D012151:Resuscitation / Q000379:methods*; D012462:Saline Solution, Hypertonic / Q000627:therapeutic use*; D012756:Sheep; D012771:Shock, Hemorrhagic / Q000378:metabolism / Q000503:physiopathology* / Q000628:therapy*; D013318:Stroke Volume / Q000187:drug effects
chemical_list: D003911:Dextrans; D004338:Drug Combinations; D012462:Saline Solution, Hypertonic